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Cardiovascular Research 1990 24(4):340-344; doi:10.1093/cvr/24.4.340
© 1990 by European Society of Cardiology
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Copyright © 1990, European Society of Cardiology

A new experimental model for measurement of pulmonary arterial haemodynamic variables in conscious rats before and after pulmonary embolism and during general anaesthesia

Günter A J Riegger and Peter Hoferer

Medizinische Universitätsklinik, Joseph Schneider Strasse 2, D-8700 Würzburg, Federal Republic of Germany

Study objective – The aim of the study was to develop a new animal model of pulmonary arterial hypertension allowing direct measurement of pulmonary artery pressure in conscious chronically instrumented rats.

Design – Pulmonary artery pressure was measured via a pulmonary artery catheter, and cardiac output by thermodilution with a thermistor probe in the aortic arch, allowing determination of stroke volume and total pulmonary arterial resistance. Pulmonary hypertension was induced by fractionated injections of latex microspheres into pulmonary circulation, causing an increase in mean pulmonary pressure of 13.7 mm Hg (p<0.001). To test the regulatory influence of the renin system on the pulmonary vascular bed, one group of rats received an intravenous bolus injection of the angiotensin converting enzyme inhibitor teprotide 1 mg·kg–1 24 h after pulmonary embolism. The effect of general barbiturate anaesthesia was also investigated.

Subjects – Experimental animals were male Wistar rats, 300-350 g weight. They were studied in groups of 6-8.

Main results – Following pulmonary embolism there was no significant difference in haemodynamic variables between control and teprotide treated rats. General anaesthesia caused an 11% fall in mean pulmonary artery pressure (p<0.01) and a 32% decrease in cardiac index (p<0.01).

Conclusions – (1) The renin-angiotensin system has no important role in the regulation of pulmonary resistance vessels 24 h after pulmonary embolism; (2) the negative inotropic effect of anaesthesia has major implications for interpretation of results obtained in animals under general anaesthesia; and (3) the results emphasise the need to study haemodynamic variables in conscious chronically instrumented, fully recovered, animals

KEYWORDS pulmonary arterial haemodynamics; pulmonary embolism; ACE inhibition

Correspondence to: Professor Riegger


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